Rostral Ventromedial Medulla (RVM) Projects to the Lateral Hypothalamic Area (LHA) to Drive Aversion and Anxiety.

Post‐inflammatory hyperpigmentation (PIH) is a common sequela of acne and may occur with or without scarring or persistent inflammation, particularly in skin of colour (SOC) individuals (Fitzpatrick Skin Types III–VI) (Figure ) [, ]. PIH can be long‐lasting. In a multicentre study, over half of the SOC participants had PIH persisting for at least 1 year, and 22.3% reported persistence for 5 years or longer. Many rated PIH as equally or more bothersome than acne itself []. This pigmentary aftermath contributes significantly to psychosocial distress even after the resolution of active acne, as facial pigmentation can affect self‐esteem, social confidence and quality of life []. PIH secondary to acne in two patients: (a) multiple hyperpigmented macules with atrophic acne scars on the cheek; (b) scattered hyperpigmented macules on the cheek without atrophic scarring. Acne develops through interacting pathways including genetic susceptibility, follicular hyperkeratinisation, excess sebum production, hormonal influences, () proliferation, inflammation and environmental exposures []. Androgens and IGF‐1 enhance sebaceous activity, while innate immune activation, such as NLRP3 inflammasome signalling, amplifies inflammation and tissue injury [, ]. These processes promote acne lesion formation.